S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas
Identifieur interne : 001797 ( Main/Exploration ); précédent : 001796; suivant : 001798S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas
Auteurs : Tracy Tucker [Canada] ; Vincent M. Riccardi [États-Unis] ; Carolyn Brown [Canada] ; John Fee [Canada] ; Margaret Sutcliffe [Canada] ; Juergen Vielkind [Canada] ; Janine Wechsler [France] ; Pierre Wolkenstein [France] ; Jan M. Friedman [Canada]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2011-09.
English descriptors
- KwdEn :
Abstract
Neurofibromatosis 1 (NF1) is an autosomal dominant disease that predisposes individuals to developing benign neurofibromas. Some features and consequences of NF1 appear to result from partial deficiency of neurofibromin (Nfn), the NF1 gene protein product, as a result of haploinsufficiency for the NF1 gene. Other features and consequences of NF1 appear to involve total deficiency of Nfn, which arises as a result of either loss of function of the second NF1 allele or excess degradation of Nfn produced by the second allele in a particular clone of cells. We used immunofluorescence to assess the presence of Nfn in putative Schwann cells (S100B+) and non‐Schwann cells (S100B−) in 36 NF1‐derived benign neurofibromas classified histologically as diffuse or encapsulated. The S100B+/Nfn− cell population made up only 18% ± 10% (mean ± standard deviation) of the neurofibroma cells in both the diffuse and encapsulated neurofibromas. The proportion of S100B+/Nfn+ cells was significantly higher and the proportion of S100B−/Nfn− cells was significantly lower in diffuse neurofibromas than in encapsulated neurofibromas. We isolated S100B+/Nfn+, S100B+/Nfn−, and S100B−/Nfn+ cells by laser microdissection and, using X‐chromosome inactivation profiles, assessed clonality for each cell type. We showed that, although some neurofibromas include a subpopulation of S100B+/Nfn− cells consistent with clonal expansion of a Schwann cell progenitor that has lost function of both NF1 alleles, other neurofibromas do not show evidence of monoclonal proliferation of Schwann cells. Our findings suggest that, although clonal loss of neurofibromin function is probably involved in the development of some NF1‐associated neurofibromas, other pathogenic processes also occur. © 2011 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jnr.22654
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 001409
- to stream Istex, to step Curation: 001409
- to stream Istex, to step Checkpoint: 000382
- to stream Main, to step Merge: 001875
- to stream Main, to step Curation: 001797
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas</title>
<author><name sortKey="Tucker, Tracy" sort="Tucker, Tracy" uniqKey="Tucker T" first="Tracy" last="Tucker">Tracy Tucker</name>
</author>
<author><name sortKey="Riccardi, Vincent M" sort="Riccardi, Vincent M" uniqKey="Riccardi V" first="Vincent M." last="Riccardi">Vincent M. Riccardi</name>
</author>
<author><name sortKey="Brown, Carolyn" sort="Brown, Carolyn" uniqKey="Brown C" first="Carolyn" last="Brown">Carolyn Brown</name>
</author>
<author><name sortKey="Fee, John" sort="Fee, John" uniqKey="Fee J" first="John" last="Fee">John Fee</name>
</author>
<author><name sortKey="Sutcliffe, Margaret" sort="Sutcliffe, Margaret" uniqKey="Sutcliffe M" first="Margaret" last="Sutcliffe">Margaret Sutcliffe</name>
</author>
<author><name sortKey="Vielkind, Juergen" sort="Vielkind, Juergen" uniqKey="Vielkind J" first="Juergen" last="Vielkind">Juergen Vielkind</name>
</author>
<author><name sortKey="Wechsler, Janine" sort="Wechsler, Janine" uniqKey="Wechsler J" first="Janine" last="Wechsler">Janine Wechsler</name>
</author>
<author><name sortKey="Wolkenstein, Pierre" sort="Wolkenstein, Pierre" uniqKey="Wolkenstein P" first="Pierre" last="Wolkenstein">Pierre Wolkenstein</name>
</author>
<author><name sortKey="Friedman, Jan M" sort="Friedman, Jan M" uniqKey="Friedman J" first="Jan M." last="Friedman">Jan M. Friedman</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:A646F27D79A74DF6EA5CAE535C9B2341C9089EF5</idno>
<date when="2011" year="2011">2011</date>
<idno type="doi">10.1002/jnr.22654</idno>
<idno type="url">https://api-v5.istex.fr/document/A646F27D79A74DF6EA5CAE535C9B2341C9089EF5/fulltext/pdf</idno>
<idno type="wicri:Area/Istex/Corpus">001409</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001409</idno>
<idno type="wicri:Area/Istex/Curation">001409</idno>
<idno type="wicri:Area/Istex/Checkpoint">000382</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000382</idno>
<idno type="wicri:doubleKey">0360-4012:2011:Tucker T:s:b:and</idno>
<idno type="wicri:Area/Main/Merge">001875</idno>
<idno type="wicri:Area/Main/Curation">001797</idno>
<idno type="wicri:Area/Main/Exploration">001797</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas</title>
<author><name sortKey="Tucker, Tracy" sort="Tucker, Tracy" uniqKey="Tucker T" first="Tracy" last="Tucker">Tracy Tucker</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia</wicri:regionArea>
<wicri:noRegion>British Columbia</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Children's and Women's Hospital, Box 153, 4500 Oak Street, Room J106, Vancouver, British Columbia</wicri:regionArea>
<wicri:noRegion>British Columbia</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Riccardi, Vincent M" sort="Riccardi, Vincent M" uniqKey="Riccardi V" first="Vincent M." last="Riccardi">Vincent M. Riccardi</name>
<affiliation wicri:level="2"><country>États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>The Neurofibromatosis Institute, La Crescenta</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Brown, Carolyn" sort="Brown, Carolyn" uniqKey="Brown C" first="Carolyn" last="Brown">Carolyn Brown</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia</wicri:regionArea>
<wicri:noRegion>British Columbia</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Fee, John" sort="Fee, John" uniqKey="Fee J" first="John" last="Fee">John Fee</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia</wicri:regionArea>
<wicri:noRegion>British Columbia</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Sutcliffe, Margaret" sort="Sutcliffe, Margaret" uniqKey="Sutcliffe M" first="Margaret" last="Sutcliffe">Margaret Sutcliffe</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia</wicri:regionArea>
<wicri:noRegion>British Columbia</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Vielkind, Juergen" sort="Vielkind, Juergen" uniqKey="Vielkind J" first="Juergen" last="Vielkind">Juergen Vielkind</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Cancer Endocrinology, BC Cancer Research Centre, Vancouver, British Columbia</wicri:regionArea>
<wicri:noRegion>British Columbia</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Wechsler, Janine" sort="Wechsler, Janine" uniqKey="Wechsler J" first="Janine" last="Wechsler">Janine Wechsler</name>
<affiliation wicri:level="3"><country xml:lang="fr">France</country>
<wicri:regionArea>Department of Pathology, Henri‐Mondor Hospital, Créteil</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Créteil</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Wolkenstein, Pierre" sort="Wolkenstein, Pierre" uniqKey="Wolkenstein P" first="Pierre" last="Wolkenstein">Pierre Wolkenstein</name>
<affiliation wicri:level="3"><country xml:lang="fr">France</country>
<wicri:regionArea>Department of Dermatology, Henri‐Mondor Hospital, Créteil</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Créteil</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Friedman, Jan M" sort="Friedman, Jan M" uniqKey="Friedman J" first="Jan M." last="Friedman">Jan M. Friedman</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia</wicri:regionArea>
<wicri:noRegion>British Columbia</wicri:noRegion>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Journal of Neuroscience Research</title>
<title level="j" type="abbrev">J. Neurosci. Res.</title>
<idno type="ISSN">0360-4012</idno>
<idno type="eISSN">1097-4547</idno>
<imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2011-09">2011-09</date>
<biblScope unit="volume">89</biblScope>
<biblScope unit="issue">9</biblScope>
<biblScope unit="page" from="1451">1451</biblScope>
<biblScope unit="page" to="1460">1460</biblScope>
</imprint>
<idno type="ISSN">0360-4012</idno>
</series>
<idno type="istex">A646F27D79A74DF6EA5CAE535C9B2341C9089EF5</idno>
<idno type="DOI">10.1002/jnr.22654</idno>
<idno type="ArticleID">JNR22654</idno>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0360-4012</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>S100B</term>
<term>benign</term>
<term>clonality</term>
<term>neurofibroma</term>
<term>neurofibromin</term>
</keywords>
</textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Neurofibromatosis 1 (NF1) is an autosomal dominant disease that predisposes individuals to developing benign neurofibromas. Some features and consequences of NF1 appear to result from partial deficiency of neurofibromin (Nfn), the NF1 gene protein product, as a result of haploinsufficiency for the NF1 gene. Other features and consequences of NF1 appear to involve total deficiency of Nfn, which arises as a result of either loss of function of the second NF1 allele or excess degradation of Nfn produced by the second allele in a particular clone of cells. We used immunofluorescence to assess the presence of Nfn in putative Schwann cells (S100B+) and non‐Schwann cells (S100B−) in 36 NF1‐derived benign neurofibromas classified histologically as diffuse or encapsulated. The S100B+/Nfn− cell population made up only 18% ± 10% (mean ± standard deviation) of the neurofibroma cells in both the diffuse and encapsulated neurofibromas. The proportion of S100B+/Nfn+ cells was significantly higher and the proportion of S100B−/Nfn− cells was significantly lower in diffuse neurofibromas than in encapsulated neurofibromas. We isolated S100B+/Nfn+, S100B+/Nfn−, and S100B−/Nfn+ cells by laser microdissection and, using X‐chromosome inactivation profiles, assessed clonality for each cell type. We showed that, although some neurofibromas include a subpopulation of S100B+/Nfn− cells consistent with clonal expansion of a Schwann cell progenitor that has lost function of both NF1 alleles, other neurofibromas do not show evidence of monoclonal proliferation of Schwann cells. Our findings suggest that, although clonal loss of neurofibromin function is probably involved in the development of some NF1‐associated neurofibromas, other pathogenic processes also occur. © 2011 Wiley‐Liss, Inc.</div>
</front>
</TEI>
<affiliations><list><country><li>Canada</li>
<li>France</li>
<li>États-Unis</li>
</country>
<region><li>Californie</li>
<li>Île-de-France</li>
</region>
<settlement><li>Créteil</li>
</settlement>
</list>
<tree><country name="Canada"><noRegion><name sortKey="Tucker, Tracy" sort="Tucker, Tracy" uniqKey="Tucker T" first="Tracy" last="Tucker">Tracy Tucker</name>
</noRegion>
<name sortKey="Brown, Carolyn" sort="Brown, Carolyn" uniqKey="Brown C" first="Carolyn" last="Brown">Carolyn Brown</name>
<name sortKey="Fee, John" sort="Fee, John" uniqKey="Fee J" first="John" last="Fee">John Fee</name>
<name sortKey="Friedman, Jan M" sort="Friedman, Jan M" uniqKey="Friedman J" first="Jan M." last="Friedman">Jan M. Friedman</name>
<name sortKey="Sutcliffe, Margaret" sort="Sutcliffe, Margaret" uniqKey="Sutcliffe M" first="Margaret" last="Sutcliffe">Margaret Sutcliffe</name>
<name sortKey="Tucker, Tracy" sort="Tucker, Tracy" uniqKey="Tucker T" first="Tracy" last="Tucker">Tracy Tucker</name>
<name sortKey="Vielkind, Juergen" sort="Vielkind, Juergen" uniqKey="Vielkind J" first="Juergen" last="Vielkind">Juergen Vielkind</name>
</country>
<country name="États-Unis"><region name="Californie"><name sortKey="Riccardi, Vincent M" sort="Riccardi, Vincent M" uniqKey="Riccardi V" first="Vincent M." last="Riccardi">Vincent M. Riccardi</name>
</region>
</country>
<country name="France"><region name="Île-de-France"><name sortKey="Wechsler, Janine" sort="Wechsler, Janine" uniqKey="Wechsler J" first="Janine" last="Wechsler">Janine Wechsler</name>
</region>
<name sortKey="Wolkenstein, Pierre" sort="Wolkenstein, Pierre" uniqKey="Wolkenstein P" first="Pierre" last="Wolkenstein">Pierre Wolkenstein</name>
</country>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Canada/explor/ParkinsonCanadaV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001797 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001797 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Canada |area= ParkinsonCanadaV1 |flux= Main |étape= Exploration |type= RBID |clé= ISTEX:A646F27D79A74DF6EA5CAE535C9B2341C9089EF5 |texte= S100B and neurofibromin immunostaining and X‐inactivation patterns of laser‐microdissected cells indicate a multicellular origin of some NF1‐associated neurofibromas }}
![]() | This area was generated with Dilib version V0.6.29. | ![]() |